Platelet GPIb and downstream activation by S. sanguis

Abstract:

There is increasing evidence suggesting the contribution of bacterial infections in atherothrombotic conditions. Studies have demonstrated that bacteria residing within the oral cavity activate platelets once they enter circulation. S. sanguis 2017-78 is capable of stimulating platelet aggregation in a thromboxane-dependent manner. In the present study, the signaling events associated with S. sanguis have been studied further. S. sanguis 2017-78 caused the phosphorylation of p38 MAP kinase and subsequently cPLA2. The p38 MAP kinase inhibitor, SB203580 inhibited S. sanguis 2017-78-induced platelet aggregation as well as the phosphorylation of both p38 MAP kinase and cPLA2. These data are consistent with cPLA2 as a physiological target of p38.
A second component of the study examined the effects of aspirin, a known inhibitor of cyclooxygenase, on these signalling pathways.